Chronic Neurological Problems

Susan Greathouse RN BN MSN

Headache
Tension-type

Bilateral location and press/tightening quality Recurring, unilateral or bilateral throbbing pain, trigger, history Repeated headaches for weeks or months

Migraine

Cluster

Seizure Disorders and Epilepsy

Seizure is a paroxysmal, uncontrolled electrical discharge of neurons in the brain that interrupts normal function Epilepsy is a condition in which a person has spontaneously recurring seizures caused by a chronic underlying cause

Generalized Seizures
Prodromal phase Aural phase Ictal phase Postictal phase

Metabolic Disturbances
Acidosis Electrolyte imbalances Hypoglycemia Hypoxia Alcohol and barbiturate withdrawal Dehydration Water intoxication

Generalized Seizures
Tonic-Clonic

Cyanosis, excessive salivation, tongue or cheek biting, incontinence Brief staring spell

Absence

Atypical absence seizures

Staring accompanied by other s&s

Other Types excessive jerk, falling

Partial Seizures
Partial focal seizures Complex partial seizures
Temporal lobe absence Automatism repetitive movements

Status Epilepticus
Ventilatory insufficiency Hypoxemia Cardiac dysrhythmias Hyperthermia Systemic acidosis Treated with Lorazepam or Diazepam

Drug Therapy
Antiseizure drugs (pg. 1538) 70% of the patients seizures are controlled Therapeutic ranges are guides for therapy, not toxic ranges

Acute Intervention
Carefully observe and record details Exact onset Course and nature, duration Autonomic signs Maintain a patent airway Do not restrain Suction and oxygen if needed

Degenerative Diseases: Multiple Sclerosis (MS)

Results from damage/scarring of myelin sheath

MS Epidemiology
Incidence
58/100,000 More common in cooler climates

Women > men Peak age of onset = 20-40 Race = Caucasian most likely to be affected (90%)

MS Pathophysiology
Unknown trigger stimulates immune response -> inflammatory response ->myelin sheath damage -> scar/plaque formation -> nerve impulse interruption

Types of MS
Relapsing-remitting Primary-progressive Secondary-progressive Progressive-relapsing

MS Assessment
History Physical assessment
Motor changes Sensory changes Cognitive changes Psychosocial changes

Labs Radiology

MS Interventions
Exercise/physical therapy Medications
Steroids Immunosuppressants Immunomodulators Cholinergics anticholinergics

Complementary therapies

Neurotransmitter Dysfunction: Parkinsons Disease

Neurotransmitter affected = Dopamine Destruction of substantia nigra = loss of dopamine Pathophysiology
Movement = balance of ACh and DA Loss of DA = loss of control of voluntary muscles

Parkinsons Disease Demographics

50,000 new cases per year Age = usually > 50 More common in men 3:2 ratio

Stages of Parkinsons Disease

Stage 1 = initial stage Stage 2 = mild symptoms Stage 3 = moderate symptoms Stage 4 = severe disability Stage 5 = complete dependence

Assessment of Parkinsons
Posture Gait Motor function Speech Autonomic dysfunction Psychosocial issues

Parkinsons: Medical Interventions

Medications
Dopaminergics Dopamine receptor agonists Anticholinergics MAO inhibitors COMT inhibitors

Physical and occupational therapy Surgical management

Parkinsons: Nursing Interventions

Safety
Medications Ambulation

Communication Nutrition Support

Neurotransmitter Dysfunction: Myasthenia Gravis (MG)

Neurotransmitter affected = ACh Pathophysiology

Auto-immune process: antibodies developed to ACh receptor sites Thymus gland abnormalities in 85% cases 0.4/100,000 Women:men = 2-3:1 Peak age of onset = 20-30

Epidemiology

Myasthenia Gravis Assessment

Physical Exam

Labs

Progressive muscle weakness Poor posture Ocular palsies Ptosis Diplopia Fatigue Loss of bowel/bladder control

Ach receptor antibodies CXR, Chest CT

Radiology

EMG Tensilon test

Myasthenia Gravis Management

Activity Planning Medications

Anticholinesterases Steroids Immunosuppressant drugs

Nutritional support Communication Eye protection Thymectomy Education

Plasmapheresis Respiratory support

Restless Legs Syndrome

Unpleasant sensory and motor abnormalities of one or both legs Cause unknown Primary family history Secondary iron deficiency, renal failure, polyneuropathy, DM, RA, pregnancy Remove aggrevating factors drug tx.

Amyotrophic Lateral Sclerosis (ALS) Lou Gehrigs

Pathophysiology
Progressive degeneration/death of motor neurons Cause = unknown; ? abnormal metabolism of glutamate

ALS Epidemiology
1.5/100,000 Men more than women 2:1 Age of onset = 40-70

ALS Assessment
Physical assessment

Fatigue while talking Tongue atrophy Dysphagia Weakness of hands/arms Nasal quality of speech Dysarthria

Labs = 0 Radiology = 0 Tests = 0 Treatment

Experimental meds

Fluorouracil Thalidomide

Huntingtons Disease
Genetic, autosomal dominant disorder 30-50 years Deficiency of neurotransmitters Ach and gama-aminobutyric acid Abnormal and excessive involuntary movements (chorea) Gait deterioration, intellectual decline, psychotic behavior

Alzheimers Disease
Most common form of dementia, chronic progressive, degenerative 5% of people 65-74 Diagnosed by presence of neurofibrillary tangles, -amyloid plaques, loss of connections between cells and cell death at autopsy

AD Early Warning Signs

Memory loss Deterioration in personal hygiene Loss of ability to concentrate and maintain attention Altered or unpredictable actions Dysphasia, apraxia, visual agnosia, dysgraphia Aggression and tendency to wander

AD Drug Therapy
Cholinesterase inhibitors Namenda Management of behavior problems
Antipsychotic drugs SSRI, TCA Antiseizure Hormones and herbs

Guillain-Barre Syndrome (GBS)

Pathophysiology
Segmental demyelination of motor neurons Inflammatory response, typically following a viral infection, acute illness, trauma, surgery, or vaccination Auto-immune process: T-cells become sensitized to myelin

GBS Epidemiology
1.9/100,000 Men = women Age of onset = 30-50, higher rates in those >50 More common in those with Hodgkins disease, SLE, HIV More common in Caucasians

GBS Physical Assessment

Motor

Sensory

Ascending symmetric weakness Decreased/absent deep tendon reflexes Respiratory compromise Loss of bowel/bladder control

Paresthesias Pain Facial weakness Dysphagia Diplopia Difficulty speaking

Cranial Nerve

GBS Assessment
Autonomic dysfunction

Labs

CSF

Labile BP Cardiac dysrhythmias tachycardia

EMG Respiratory function studies

GBS Interventions
Medications

Supportive

ACTH Immunoglobins

Plasmapheresis

Pulmonary Immobility Pain Communication ADLs